The identity and topographic localization of immunocompetent cells and the alteration of surface markers on ocular resident cells in animals with vari s experimental uveitis were analyzed by immunohistochemical studies and in situ hybridization. Previously, we have demonstrated that T lymphocytes were the predominantly infiltrating cells in experimental autoimmune uveoretinitis (EAU), yet both macrophages and polymorphonuclear neutrophils were the predominantly infiltrating cells in endotoxin-induced uveitis (EIU). Cytokines (e.g., gamma-interferon), inflammatory mediators (e.g., nitric oxide), and some retinal proteins (e.g., S-antigen (S-Ag)) pl an important role in the immunopathogenesis of EAU and EIU. Agents that modulate them can alter the immunopathology of the experimental model. For example, prolonged corticosteroid therapies enhance S-Ag expression in nonretinal ocular tissues of rats with EAU. Several new animal models, including experimental melanin-protein-induced uveitis (EMIU), experimental blepharitis, murine allergic conjunctivitis, a murine toxoplasmosis, have been developed and studied. They represented different entities of uveitis in humans. EMIU closely resembles Vogt- Kayanagi-Harada syndrome and sympathetic ophthalmia; experimental blepharitis induced by immunization of monoclonal antibody of Id16/6 resembles idiopathic blepharitis; murine allergic conjunctivitis induced by compound 48/80 resembles allergic conjunctivitis; murine toxoplasmosis infected with T. gondii resembles acquired ocular toxoplasmosis. Specimens from human ocular tissues with various diseases, including uveitis, retinal and corneal diseases, tumors, and metabolic genetic disorders, are studied using immunohistochemical and in situ hybridization techniques as well as light and electron microscopic examinations. In uveitis, immunocompetent cells and lymphokines besides the stimulators (e.g infectious organisms) are valuable adjuncts to the clinical diagnosis and t understanding of pathogenesis of the diseases. In nonuveitic conditions, alteration of cellular membrane surface markers and intracytoplasmic organelles of the ocular resident cells (e.g., crystalline inclusions in Be ti's crystalline dystrophy; B-cell marker in intraocular lymphoma) may reflect cellular damage and abnormalities in these diseases. Elucidating the immunopathological role of the relationships between infiltrating inflammat y or malignant cells and other resident cells in the clinical behavior of various diseases will increase our understanding of human ocular disorders and provide better treatment.